Suppr超能文献

前列环素和伊洛前列素诱导的心肌缺血。

Myocardial ischemia induced by prostacyclin and iloprost.

作者信息

Bugiardini R, Galvani M, Ferrini D, Gridelli C, Tollemeto D, Mari L, Puddu P, Lenzi S

出版信息

Clin Pharmacol Ther. 1985 Jul;38(1):101-8. doi: 10.1038/clpt.1985.142.

Abstract

Vasodilators of resistive vessels may induce ischemia in patients with coronary artery disease. To evaluate this possibility during prostacyclin (PGI2; scalar doses up to 10 ng/kg/min) and prostacyclin analog (iloprost; scalar doses up to 6 ng/kg/min) infusions, we studied 33 patients with angina pectoris and proved coronary artery disease. Patients were also submitted to dipyridamole (0.15 mg/kg/min for 4 minutes) and exercise stress testing (starting at 25 W and increasing 25 W every 2 minutes). In a preliminary study the hemodynamic and side effects of iloprost were studied in seven healthy subjects. At an iloprost dose of 4 to 6 ng/kg/min, these subjects had a significant decrease in mean arterial pressure and total peripheral and pulmonary vascular resistances. Side effects were limited to facial flushing and slight headache and were readily reversible. PGI2 induced typical chest pain and significant ST segment depression in six patients with severe coronary artery disease (three with left main and three with triple vessel disease) and poor exercise tolerance (means +/- SD = 362 +/- 99 seconds). All six patients had had angina during the dipyridamole infusion. Similar findings were observed after iloprost infusion in four of these. Aminophylline (125 mg iv) completely relieved chest pain. Although the rate-pressure products occasionally rose during PGI2 and iloprost infusions, there were no significant changes between ischemic (11.3 +/- 2.3 and 10.6 +/- 1.4 X 10(-3) U) and preischemic (10.8 +/- 1.5 and 10.7 +/- 1.4 X 10(-3) U) rates of infusion. Our data indicate that PGI2 and iloprost may induce ischemia independently of changes in oxygen demand, and suggest that these drugs dilate small coronary vessels. This may result in decreased subendocardial perfusion pressure and/or "coronary steal."

摘要

阻力血管扩张剂可能会诱发冠状动脉疾病患者发生缺血。为评估在输注前列环素(PGI2;剂量高达10 ng/kg/min)和前列环素类似物(依洛前列素;剂量高达6 ng/kg/min)期间出现这种可能性,我们研究了33例患有心绞痛且已证实患有冠状动脉疾病的患者。患者还接受了双嘧达莫(0.15 mg/kg/min,持续4分钟)和运动负荷试验(起始功率25 W,每2分钟增加25 W)。在一项初步研究中,对7名健康受试者研究了依洛前列素的血流动力学及副作用。当依洛前列素剂量为4至6 ng/kg/min时,这些受试者的平均动脉压、总外周血管阻力和肺血管阻力显著降低。副作用仅限于面部潮红和轻微头痛,且易于逆转。PGI2在6例患有严重冠状动脉疾病(3例左主干病变和3例三支血管病变)且运动耐量差(平均值±标准差 = 362 ± 99秒)的患者中诱发了典型胸痛和显著的ST段压低。所有6例患者在输注双嘧达莫期间均有心绞痛发作。其中4例在输注依洛前列素后观察到类似结果。氨茶碱(静脉注射125 mg)完全缓解了胸痛。尽管在输注PGI2和依洛前列素期间心率 - 血压乘积偶尔会升高,但缺血时(11.3 ± 2.3和10.6 ± 1.4×10⁻³ U)与缺血前(10.8 ± 1.5和10.7 ± 1.4×10⁻³ U)的输注速率之间无显著变化。我们的数据表明,PGI2和依洛前列素可能独立于氧需求变化而诱发缺血,并提示这些药物可扩张冠状动脉小血管。这可能导致心内膜下灌注压降低和/或“冠状动脉窃血”。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验